Specialized groups of cardiac cells that form the cardiac conduction system control the frequency, pathway of conduction, and rate of propagation of action potentials through the heart, which cause the heart to beat in an efficient manner. This special conduction system includes the sinoatrial node (SA node), the atrial internodal tracts, the atrioventricular node (AV node), the His bundle, and the right and left bundle branches.
The SA node, located at the junction of the superior vena cava and right atrium, normally acts as the natural pacemaker, generating action potentials, which are conducted through the rest of the heart. When normal conduction pathways are intact, an action potential generated in the SA node is conducted through the atria and to the AV node via the atrial internodal tracts. The conduction through the AV nodal tissue takes longer than through the atrial tissue, resulting in a delay between atrial contraction and the start of ventricular contraction.
The AV node, located in the central fibrous body, conducts the action potential to the His bundle, located under the annulus of the tricuspid valve. The His bundle splits into the left and right bundle branches, which conduct the action potential to specialized fibers called “Purkinje fibers.” The bundle branches rapidly conduct the action potential down the ventricular septum, where the Purkinje fibers spread the depolarization wavefront quickly to the remaining ventricular myocardium, producing a coordinated contraction of the ventricular muscle mass.
Conduction abnormalities may cause slowed or disrupted conduction anywhere along this conduction pathway. For example, the SA node may not generate action potentials at a fast enough rate resulting in too slow of heart rate, or bradycardia. AV block may prevent conduction of the action potential from the atria to the ventricles. A left and right bundle branch block, or other conduction abnormalities in the Purkinje fibers or ventricular myocardium, may cause the contraction of the right and left ventricles to be asynchronous. These and other conduction abnormalities may be treated by an external or implantable pacemaker.
Pacemakers are typically coupled to the heart via one or more implantable leads, each carrying one or more electrodes for stimulating the heart and for sensing the intrinsic electrical signals associated with a conducted action potential. Electrodes are commonly placed on the endocardial surface using a transvenous approach. For example, a right ventricular lead may be advanced into the right ventricle and placed such that an electrode is positioned at or near the right ventricular apex. Low capture thresholds and stable lead positioning have made the right ventricular apex a preferred ventricular stimulation site.
However, ventricular pacing at the location of the right ventricular apex does not mimic the normal ventricular conduction pathway. Both experimental and clinical studies have shown that septal pacing can improve various indices of cardiac function compared to apical pacing. Direct myocardial stimulation, as occurs in apical pacing, can cause remodeling of the ventricular myocardium, including myofibrilar disarray and local hypertrophy away from the electrode.
The most normal physiological approach to pacing the ventricles when normal AV nodal conduction fails may be to deliver electrical stimulation pulses directly to the His bundle. Depolarization of the His bundle tissue may be conducted normally through the ventricular conduction pathway, down the left and right bundle branches and to the remainder of the ventricular myocardium. The resulting ventricular contraction, which is more rapid and results in a narrow QRS complex and a more vigorous, normal contraction, may produce a better-coordinated ventricle contraction for achieving efficient heart pumping action.
In some cases, left ventricular (LV) pacing/sensing may be desired instead of, or in addition to right ventricular (RV) pacing/sensing. For example, RV and LV pacing may be provided in a time coordinated fashion to resynchronize the contraction of the ventricles, e.g., provide cardiac resynchronization therapy (CRT), which may be indicated for cardimyopathy or other ventricular conduction abnormalities. For LV pacing/sensing, a lead may be transvenously advanced through the right ventricle, into the coronary sinus and, in some cases, a coronary vein branching from the coronary sinus, to place electrodes near the myocardium of the left ventricle.
Leads may also be transvenously implanted in one or both atria. Furthermore, in some cases, cardiac pacing/sensing leads cannot be, or for some other reason are not implanted transvenously. In such cases, a lead may be epicardially implanted by fixing an electrode at the distal tip of the lead to the myocardium through an incision or puncture in the pericardium.